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Wednesday, September 26, 2012

Breast Cancer Further Demystified Exposes Importance of Before Forty Initiative

Breast cancer has been further demystified genetically, which will lead to better, more targeted treatments. The take home message is clear: More work needs to be done on the genomic front lines of breast cancer research.

Important to note: The findings clearly indicate that triple negative breast cancer is found in young women, particularly African-American women. Our Before Forty Initiative has been fighting for four years to promote this fact. Please read more about how you can help Here.

From the New York Times:

Study Divides Breast Cancer Into Four Distinct Types

By
GINA KOLATA

In findings that are fundamentally reshaping the scientific understanding of breast cancer, researchers have identified four genetically distinct types of the cancer. And within those types, they found hallmark genetic changes that are driving many cancers.

These discoveries, published online on Sunday in the journal Nature,
are expected to lead to new treatments with drugs already approved for
cancers in other parts of the body and new ideas for more precise
treatments aimed at genetic aberrations that now have no known
treatment.

The study is the first comprehensive genetic analysis of breast cancer,
which kills more than 35,000 women a year in the United States. The new
paper, and several smaller recent studies, are electrifying the field.

“This is the road map for how we might cure breast cancer in the
future,” said Dr. Matthew Ellis of Washington University, a researcher
for the study.

Researchers and patient advocates caution that it will still take years
to translate the new insights into transformative new treatments. Even
within the four major types of breast cancer, individual tumors
appear to be driven by their own sets of genetic changes. A wide
variety of drugs will most likely need to be developed to tailor
medicines to individual tumors.

“There are a lot of steps that turn basic science into clinically
meaningful results,” said Karuna Jaggar, executive director of Breast Cancer Action, an advocacy group. “It is the ‘stay tuned’ story.”

The study is part of a large federal project, the Cancer Genome Atlas, to build maps of genetic changes in common cancers. Reports on similar studies of lung and colon cancer have been published recently. The breast cancer study was based on an analysis of tumors from 825 patients.

“There has never been a breast cancer genomics project on this scale,”
said the atlas’s program director, Brad Ozenberger of the National Institutes of Health.

The investigators identified at least 40 genetic alterations that might
be attacked by drugs. Many of them are already being developed for other
types of cancer that have the same mutations. “We now have a good view
of what goes wrong in breast cancer,” said Joe Gray, a genetic expert at
Oregon Health & Science University, who was not involved in the study. “We haven’t had that before.”

The study focused on the most common types of breast cancer that are
thought to arise in the milk duct. It concentrated on early breast
cancers that had not yet spread to other parts of the body in order to
find genetic changes that could be attacked, stopping a cancer before it
metastasized.

The study’s biggest surprise involved a particularly deadly breast cancer whose tumor
cells resemble basal cells of the skin and sweat glands, which are in
the deepest layer of the skin. These breast cells form a scaffolding for
milk duct cells. This type of cancer is often called triple negative
and accounts for a small percentage of breast cancer.

But researchers found that this cancer was entirely different from the other types of breast cancer and much more resembles ovarian cancer and a type of lung cancer.

“It’s incredible,” said Dr. James Ingle of the Mayo Clinic, one of the
study’s 348 authors, of the ovarian cancer connection. “It raises the
possibility that there may be a common cause."

There are immediate therapeutic implications. The study gives a biologic
reason to try some routine treatments for ovarian cancer instead of a
common class of drugs used in breast cancer known as anthracyclines.
Anthracyclines, Dr. Ellis said, “are the drugs most breast cancer
patients dread because they are associated with heart damage and
leukemia.”

A new type of drug, PARP inhibitors, that seems to help squelch ovarian
cancers, should also be tried in basal-like breast cancer, Dr. Ellis
said.

Basal-like cancers are most prevalent in younger women, in
African-Americans and in women with breast cancer genes BRCA1 and BRCA2.

Two other types of breast cancer, accounting for most cases of the
disease, arise from the luminal cells that line milk ducts. These
cancers have proteins on their surfaces that grab estrogen,
fueling their growth. Just about everyone with estrogen-fueled cancer
gets the same treatment. Some do well. Others do not.

The genetic analysis divided these cancers into two distinct types.
Patients with luminal A cancer had good prognoses while those with
luminal B did not, suggesting that perhaps patients with the first kind
of tumor might do well with just hormonal therapy to block estrogen from
spurring their cancers while those with the second kind might do better
with chemotherapy in addition to hormonal therapy.

In some cases, genetic aberrations were so strongly associated with one
or the other luminal subtype that they appeared to be the actual cause
of the cancer, said Dr. Charles Perou of the University of North
Carolina, who is the lead author of the study. And he called that “a
stunning finding.”

“We are really getting at the roots of these cancers,” he said.

After basal-like cancers, and luminal A and B cancers, the fourth type
of breast cancer is what the researchers called HER2-enriched. Breast
cancers often have extra copies of a gene, HER2, that drives their
growth. A drug, Herceptin, can block the gene and has changed the
prognosis for these patients from one of the worst in breast cancer to
one of the best.

Yet although Herceptin is approved for every breast cancer patient whose
tumor makes too much HER2, the new analysis finds that not all of these
tumors are alike. The HER2-enriched should respond readily to
Herceptin; the other type might not.

The only way to know is to do a clinical trial, and one is already being
planned. Herceptin is expensive and can occasionally damage the heart.
“We absolutely only want to give it to patients who can benefit,” Dr.
Perou said.

For now, despite the tantalizing possibilities, patients will have to
wait for clinical trials to see whether drugs that block the genetic
aberrations can stop the cancers. And it could be a vast undertaking to
get all the drug testing done. Because there are so many different ways a
breast cancer cell can go awry, there may have to be dozens of drug
studies, each focusing on a different genetic change.

One of Dr. Ellis’s patients, Elizabeth Stark, 48, has a basal-type
breast cancer. She has gone through three rounds of chemotherapy,
surgery and radiation over the past four years. Her disease is stable
now and Dr. Stark, a biochemist at Pfizer, says she knows it will take
time for the explosion of genetic data to produce new treatments that
might help her.

“In 10 years it will be different,” she said, adding emphatically, “I know I will be here in 10 years.”

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